The Determination of Uneven Pulmonary Blood Flow from the Arterial Oxygen Tension During Nitrogen Washout

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The Determination of Uneven Pulmonary Blood Flow from the Arterial Oxygen Tension During Nitrogen Washout THE DETERMINATION OF UNEVEN PULMONARY BLOOD FLOW FROM THE ARTERIAL OXYGEN TENSION DURING NITROGEN WASHOUT Theodore N. Finley J Clin Invest. 1961;40(9):1727-1734. https://doi.org/10.1172/JCI104395. Research Article Find the latest version: https://jci.me/104395/pdf THE DETERMINATION OF UNEVEN PULMONARY BLOOD FLOW FROM THE ARTERIAL OXYGEN TENSION DURING NITROGEN WASHOUT By THEODORE N. FINLEY * (From the Cardiovascular Research Institute, University of California Medical School, San Francisco, Calif.) (Submitted for publication January 3, 1961; accepted May 29, 1961) Many tests are available for measuring un- lungs. The test requires the use of a nitrogen evenness of pulmonary ventilation. In recent meter and a flow-through cuvet 02 electrode for years tests of unevenness of pulmonary blood measuring arterial Po2 continuously during the flow have been described, which utilize radio- inhalation of 02. In practice the test takes ap- active krypton (1) in patients with emphysema, proximately 20 minutes and the calculations radioactive oxygen in patients with mitral steno- another 20 minutes. This method is based on sis (2), and radioactive carbon dioxide in normal the principle that the rate of rise of alveolar 02 subjects (3). These studies provide quantita- tension during oxygen inhalation depends on the tive data on the degree of unevenness of pul- distribution of inspired 02 to well and poorly monary blood flow but require expensive and ventilated regions of the lung (in relation to complicated apparatus and are not easily their volume), while the rate of simultaneous adapted to clinical pulmonary function testing. rise of arterial 02 tension depends on the dis- Simpler methods of estimating unevenness of tribution of pulmonary blood flow to these blood flow in relation to ventilation have been regions and the anatomical shunts. The theory, suggested. These are based on the rate of rise method and results of these studies in normal of arterial oxygen saturation (ear oximeter) subjects and in patients with cardiac and pul- during the inhalation of oxygen (4-6), analysis monary disease are presented here. of gas samples obtained from various lobes of the lungs (7), continuous analysis of a single THEORY expiration (8), and the difference between the The lungs can be divided into a well ventilated region nitrogen tension of alveolar gas and urine (9, (which need not be homogeneous) and a poorly ventilated 10). These simpler methods do not provide region (subscripts 1 and 2, respectively). Arterial blood quantitative data on the degree of unevenness of is a mixture of blood that has passed through these regions or through venous-to-arterial shunts. Its oxygen content pulmonary blood flow. (Ca) is related to the blood flows through the capillaries of An ingenious graphical method of determining the various regions (Q1, Q2) and through the shunt (Q8), unevenness of perfusion of the lung in patients and to their respective oxygen contents (Cl, C2 and Cv) as with chronic pulmonary emphysema has been follows: worked out by Briscoe and co-workers (11). Ca QT = C1 Q1 + C2Q2 + CQ9 [1] This method utilizes a nitrogen washout and where Qi + Q2 + Qs = QT, the cardiac output. In this wash-in technique and the arterial saturation and subsequent formulations we omit, from our otherwise (luring air-breathing. Its disadvantage is that conventional (12) symbolization, the subscript c for capil- lary and the chemical subscript 02- other causes of arterial desaturation i.e., shunts It follows from Equation 1 that at any time (t) during and diffusion barriers cause an overestimation the N2 washout: of the degree of unevenness of perfusion. In this laboratory we have devised a test Cat = C (t( ) +C2t which yields quantitative data for the deter- Q1 +Q2 Q1 +Q2 mination of the fractional alveolar ventilation (C. C.,) t -. 0.1. [2] and pulmonary capillary blood flow that go to Ql + Q2 the well and poorly ventilated regions of the Wre assume the following are constant in the later stages of the N2 washout: 1) the magnitude of the various blood * Fellow of the National Tuberculosis Association. Sup- flOwS (QI, Q2, Q., QT) relative to each other; 2) the arteri- ported in part by ITSPHS Grant H-4029. ov5eiious 02) content difference (Ca - Cv). When we then 1 727 1728 THEODORE N. FINLEY consider the difference between the final equilibrium state lated region, because the assumptions that allow the cal- at time f and the changing state at time t, it follows that: culation of PEN2 are not valid in the early portion of the N2 washout. The distribution of pulmonary blood flow is Caf - Cat = (Cf -C1)CIO matched with the distribution of alveolar ventilation when the fractional perfusion equals the fractional ventilation of the poorly ventilated region. + (C2f - C2t) ( QQ Q ) [3] The dilution index. A template was made in which log II/El + (1/n)]hn is plotted against n. This was laid Late in the washout when hemoglobin is fully saturated over the semilogarithmically plotted data and analyzed in all parts of the lung, further changes in 02 content are into linear components (16, 17) (Figure 1). The inter- linearly related to changes in 02 tension (13). Equation 3 section of the curved template with each straight line gives can then be formulated in terms of differences in Po2: a value of n (on the baseline) which is the dilution index. This index, which is related to the turnover rate (k) of Paf - Pat = (Pif - Pit) ( Q + ) Robertson, Siri and Jones (16) is the ratio FRC/VT - VD for each region. The use of the dilution index and its determination by a + (32f - P2f) (. Q Q )E[4] template has proved to be a useful shortcut in the calcula- tion of the functional residual capacity (FRC) and alveolar Any Po2 gradient due to diffusion difficulty becomes in- tidal volumes of the well and poorly ventilated regions. finitesimal at this time when Po2 is high in all alveoli It also provides a simple characterization of the alveolar (13-15). Alveolar and end-capillary oxygen tensions are ventilation of any region. thus identical within a region; i.e., PAI = Pi, PA2 =P2. Mixed expired alveolar versus end-tidal nitrogen concen- If Pco2 is constant within each region, then Po2 is related trations. In our study we measured end-tidal N2 concen- to PN2, provided that the total pressure of all gases is con- stant, as it is, in each region, and hemoglobin is fully satu- rated, as it is, at this time. Then: Paf - Pat = AP1N2 (+.0 ) + AP2N2 (CQ2) = APCN2 [5] where the various values of APN2 are the excess at time t over the final' value at timef. APCN2 is the mean value of this excess in mixed end-capillary blood. This relation holds, regardless of the number of regions. Late in the washout the concentration of nitrogen has become negligible in all but the worst ventilated region. The contributions of N2 from the inspired 02 tank and front the tissues are virtually constant; while they affect the final value they are of no significance in these considera- tions of the changes in PN2. It follows that, late in the washout: VAT APAN2 = VA2* APA2N2 and QT APaN2 = QO2AP2N2, where the subscript T refers to total alveolar ventilation or total cardiac output. Since APA2N2 = AP2N,, these two equations yield the ratio between those fractions of total alveolar ventilation and total perfusion, respectively, which are distributed to the poorly ventilated region: NO. OF BREATHS = (VA2/VAT)/(Q2/QT) APAN2/APCN2 [6] FIG. 1. PERCENTAGE OF N2 CONCENTRATION IN END- At the end of the N2 washout this ratio is constant, since EIXPIRED GAS ON LOGARITHMIC SCALE PLOTTED AGAINST semilogarithmically plotted values of APXN, and APCN2 are NUMBER OF BREATHS FOR THE WELL AND POORLY VENTI- LATED REGIONS OF THE LUNG. The dotted lines found to lie on parallel lines. When (VA2/VAT), APAN2 represent and APCN2 are experimentally determined, Q2/QT can be the N2 washouts of the well and poorly ventilated com- calculated. No attempt has been made to estimate the partments obtained from the N2 end-tidal washout. The distribution of perfusion to compartments in the well venti- dilution index template is superimposed on these graphs, giving an intercept value with the well ventilated region For present purposes we consider N2 washout complete at breath 5 and with the poorly ventilated region at breath when the forced end-expired PN2 is less than 4 mnmi Hg. 20. 1729 DETERNIINATION' OF UTNEVEN PUTLMIONARY BLOOD FLOW\ FIG. 2. RIGHT, CLARK 02 ELECTRODE (A) IN LUCITE JACKET (B) AND LEFT, THE FLOW-THROUGH CUVET (C-D) FOR THE ELECTRODE SHOWING THE HOLES (E) THAT ALLOW CIRCULATION THROUGH TUBES (F AND G) FROM THE WATERBATH AROUND CUVET AND ELECTRODE. The left-hand part fits snugly beneath the right-hand part and the membrane of the Clark electrode is in the flowing blood stream. The fact that these concentrations exceed mixed of the N2 washout on a Severinghaus modification of the tration. in this alveolar and mixed expired concentrations does not affect Clark 02 electrode (19). The Clark electrodes used over the 0 to 95 per cent 02 our determination of the dilution indices nl and n2 (18). study were slightly alinear 21 per cent 02, But this fact does necessitate the use of an additional piece range. This alinearity occurred below in determining the absolute volumes and which affected the accuracy of the Po2 record in the earlier of information deter- ventilations of the various regions. We hav-e used the part of each study but not in the later part used in to determine alveolar *ventilation mining the distribution of perfusion.
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